The regulation of the n-3 DPA derived protectins followed similar dynamics as those observed for the DHA-derived congeners, whereby PD2n-3 DPA and the protectin pathway marker 10S,17S-diHDPA, increased by three-fold and ten-fold, respectively, in STEMI patients at onset of MI compared with stable CAD and controls with normalization during follow up (Fig. 4b). This evidence concerns the gene CD59 and coronary artery disorder.